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@@ -74,7 +74,17 @@ cells to ML-162 treatment. Finally, we demonstrated that p53-mutation correlates
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  Conclusions: This study demonstrates that p53-mutant TNBC cells have critical, unique survival pathways that can be effectively targeted. \
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  Our results illustrate the intrinsic vulnerability of p53-mutant TNBCs to ferroptosis, and highlight GPX4 as a promising target for the \
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  precision treatment of p53-mutant triple-negative breast cancer."
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- ]]
 
 
 
 
 
 
 
 
 
 
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  def gradio():
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  Conclusions: This study demonstrates that p53-mutant TNBC cells have critical, unique survival pathways that can be effectively targeted. \
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  Our results illustrate the intrinsic vulnerability of p53-mutant TNBCs to ferroptosis, and highlight GPX4 as a promising target for the \
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  precision treatment of p53-mutant triple-negative breast cancer."
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+ ],
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+ ["T cells acquire a regulatory phenotype when their T cell antigen receptors (TCRs) experience an intermediate- to high-affinity \
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+ interaction with a self-peptide presented via the major histocompatibility complex (MHC). Using TCRβ sequences from flow-sorted human cells, \
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+ we identified TCR features that promote regulatory T cell (Treg) fate. From these results, we developed a scoring system to quantify TCR-intrinsic \
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+ regulatory potential (TiRP). When applied to the tumor microenvironment, TiRP scoring helped to explain why only some T cell clones maintained the \
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+ conventional T cell (Tconv) phenotype through expansion. To elucidate drivers of these predictive TCR features, we then examined the two elements of the \
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+ Treg TCR ligand separately: the self-peptide and the human MHC class II molecule. These analyses revealed that hydrophobicity in the third \
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+ complementarity-determining region (CDR3β) of the TCR promotes reactivity to self-peptides, while TCR variable gene (TRBV gene) usage shapes the TCR’s \
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+ general propensity for human MHC class II-restricted activation."
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+ ]
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+ ]
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  def gradio():
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